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H J Park - One of the best experts on this subject based on the ideXlab platform.
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Effects of GABA on pancreatic Exocrine Secretion of rats.
Journal of Korean medical science, 2020Co-Authors: H S Park, H J ParkAbstract:Since GABA and its related enzymes had been determined in beta-cells of pancreas islets, effects of GABA on pancreatic Exocrine Secretion were investigated in the isolated perfused rat pancreas. GABA, given intra-arterially at concentrations of 3, 10, 30 and 100 microM, did not exert any influence on spontaneous or secretin (12 pM)-induced pancreatic Exocrine Secretion. However, GABA further elevated cholecystokinin (10 pM)-, gastrin-releasing peptide (100 pM)- or electrical field stimulation-induced pancreatic Secretions of fluid and amylase, dose-dependently. The GABA-enhanced CCK-induced pancreatic Secretions were completely blocked by bicuculline (10 microM), a GABAA receptor antagonist but not affected by saclofen (10 microM), a GABA(B) receptor antagonist. The enhancing effects of GABA (30 microM) on CCK-induced pancreatic Secretions were not changed by tetrodotoxin (1 microM) but partially reduced by cyclo-(7-aminoheptanonyl-Phe-D-Trp-Lys-Thr[BZL]) (10 microM), a somatostatin antagonist. In conclusion, GABA enhances pancreatic Exocrine Secretion induced by secretagogues, which stimulate enzyme Secretion predominantly, via GABA(A) receptors in the rat pancreas. The enhancing effect of GABA is partially mediated by inhibition of islet somatostatin release. GABA does not modify the activity of intrapancreatic neurons.
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Roles of Gonadal Steroids on Exocrine Secretion of Isolated Perfused Rat Pancreas
The Korean Journal of Physiology and Pharmacology, 2020Co-Authors: H S Park, H J ParkAbstract:To clarify the roles of gonadal steroids on pancreatic Exocrine Secretion, effects of progesterone and estradiol-17β on spontaneous and secretagogue-induced Exocrine response of isolated perfused rat pancreas were investigated. Intra-arterial infusion of progesterone resulted in significant increase of the spontaneous pancreatic fluid and amylase Secretion dose-dependently. However, estradiol-17β did not exert any influence on spontaneous pancreatic Exocrine Secretion. Exogenous secretin, cholecystokinin (CCK), and acetylcholine markedly stimulated pancreatic fluid and amylase Secretion. Progesterone initially enhanced secretin-induced amylase Secretion, but this stimulatory response declined thereafter to basal value. Moreover, secretin-induced fluid Secretion was not affected by infusion of progesterone. Therefore, initial increase of Secretion-induced amylase Secretion by progesterone seems to be a non-specific action by washout effect of secretin. Estradiol-17β failed to change the secretin-induced fluid and amylase Secretion. Both progesterone and estradiol-17β did not exert any influence on CCK-induced fluid and amylase Secretion. Acetylcholine-induced Exocrine Secretion of isolated perfused pancreas also was not affected by intra-arterial infusion of progesterone or estradiol-17β. It is concluded from the above results that progesterone could enhance the spontaneous pancreatic fluid and amylase Secretion of isolated perfused rat pancreas through non-genomic short- term action, and that these effects could be masked by more potent stimulants such as secretin, CCK, and acetylcholine.
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γ-aminobutyric acid secreted from islet β-cells modulates Exocrine Secretion in rat pancreas
World Journal of Gastroenterology, 2006Co-Authors: Yong-deuk Park, H S Park, Guang Wu, H J ParkAbstract:AIM: To investigate the role of endogenous γ-amino-butyric acid (GABA) in pancreatic Exocrine Secretion. METHODS: The isolated, vascularly perfused rat pancreas was employed in this study to eliminate the possible influences of extrinsic nerves and hormones. Cholecystokinin (CCK; 10 pmol/L) was intra-arterially given to stimulate Exocrine Secretion of the pancreas. RESULTS: Glutamine, a major precursor of GABA, which was given intra-arterially at concentrations of 1, 4 and 10 mmol/L, dose-dependently elevated the CCK-stimulated Secretions of fluid and amylase in the normal pancreas. Bicuculline (10 μmol/L), a GABAA receptor antagonist, blocked the enhancing effect of glutamine (4 mmol/L) on the CCK-stimulated Exocrine Secretions. Glutamine, at concentrations of 1, 4 and 10 mmol/L, dose-dependently increased the GABA concentration in portal effluent of the normal pancreas. The effects of glutamine on the CCK-stimulated Exocrine Secretion as well as the GABA Secretion were markedly reduced in the streptozotocin-treated pancreas. CONCLUSION: GABA could be secreted from β-cells into the islet-acinar portal system after administration of glutainine, and could enhance the CCK-stimulated Exocrine Secretion through GABAA receptors. Thus, GABA in islet β-cells is a hormone modulating pancreatic Exocrine Secretion.
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Effects of γ-Aminobutyric acid on action of gastrin-releasing peptidergic neurons in Exocrine Secretion of isolated, perfused rat pancreas
Pancreas, 2002Co-Authors: Yong-deuk Park, H J ParkAbstract:Introduction: γ-Aminobutyric acid (GABA) has been reported to enhance Exocrine Secretion evoked by intrinsic neuronal excitation in the pancreas. Aim: To see the effect of GABA on the action of gastrin-releasing peptide (GRP)ergic neurons in Exocrine Secretion of the pancreas. Methodology: Pancreatic neurons were excited by electrical field stimulation (EFS) in the isolated, perfused rat pancreas. GRP in the pancreatic circulation was neutralized by an anti-GRP antiserum to block GRPergic neuronal action on pancreatic Exocrine Secretion. Results: GABA (3, 10, 30 μM), given intra-arterially, elevated the EFS-evoked pancreatic Secretions of fluid and amylase dose-dependently. An anti-GRP antiserum (10 μL/mL: titer of 1:66,000) reduced the GABA (10 μM)-enhanced EFS-evoked pancreatic Secretions. Synthetic porcine GRP-27 (30, 100, 300 pM) increased the pancreatic Secretions dose-dependently, and these were further elevated by GABA (10 μM). The anti-GRP antiserum also reduced the GABA-enhanced GRP (100 pM)-induced pancreatic Secretions. Bicuculline (10 μM) reduced the enhancing effect of GABA on pancreatic Secretions evoked by EFS as well as GRP. Conclusion: GABA enhances pancreatic Secretions evoked by EFS as well as GRP, which is reduced by the anti-GRP antiserum. The enhancing effects of GABA on the EFS- and GRP-induced pancreatic Secretions are diminished by bicuculline. The results indicate that GABA enhances intrinsic GRPergic neuronal action on Exocrine Secretion via the GABA A receptors in the rat pancreas.
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Endogenous somatostatin inhibits interaction of insulin and cholecystokinin on Exocrine Secretion of isolated, perfused rat pancreas
Pancreas, 2002Co-Authors: H S Park, Yong-deuk Park, Hyo Seop Yoon, H J ParkAbstract:Introduction: Although somatostatin inhibits pancreatic Exocrine Secretion, the inhibitory mechanism of endogenous somatostatin is not clearly understood. Aim: To investigate the effect of endogenous somatostatin on the interaction between endogenous insulin and exogenous cholecystokinin (CCK) in Exocrine Secretion of the totally isolated, perfused rat pancreas. Methodology: Endogenous releases of somatostatin and insulin were induced by 18 mM glucose. Streptozotocin (75 mg/kg) or cysteamine (300 mg/kg) was injected into rats 24 hours before the experiment to deplete insulin or somatostatin in the pancreas. Results: Glucose (18 mM) enhanced CCK (10 pM)-stimulated Secretions of fluid and amylase in the normal pancreas, which was further elevated by a somatostatin antagonist. Exogenous insulin (100 nM) also enhanced CCK-stimulated Secretions in the streptozotocin-treated pancreas, which was also markedly increased by the somatostatin antagonist. The glucose (18 mM)-enhanced CCK-stimulated Secretions were much higher in the cysteamine-treated pancreas than in the normal pancreas, which was dose-dependently reduced by exogenous somatostatin (30, 100 pM). However, endogenous or exogenous somatostatin did not modify the pancreatic responses to CCK alone. Conclusion: Endogenous somatostatin inhibits the interaction of endogenous insulin and CCK on pancreatic Exocrine Secretion in the rat rather than reducing the action of CCK alone or endogenous release of insulin.
H S Park - One of the best experts on this subject based on the ideXlab platform.
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Effects of GABA on pancreatic Exocrine Secretion of rats.
Journal of Korean medical science, 2020Co-Authors: H S Park, H J ParkAbstract:Since GABA and its related enzymes had been determined in beta-cells of pancreas islets, effects of GABA on pancreatic Exocrine Secretion were investigated in the isolated perfused rat pancreas. GABA, given intra-arterially at concentrations of 3, 10, 30 and 100 microM, did not exert any influence on spontaneous or secretin (12 pM)-induced pancreatic Exocrine Secretion. However, GABA further elevated cholecystokinin (10 pM)-, gastrin-releasing peptide (100 pM)- or electrical field stimulation-induced pancreatic Secretions of fluid and amylase, dose-dependently. The GABA-enhanced CCK-induced pancreatic Secretions were completely blocked by bicuculline (10 microM), a GABAA receptor antagonist but not affected by saclofen (10 microM), a GABA(B) receptor antagonist. The enhancing effects of GABA (30 microM) on CCK-induced pancreatic Secretions were not changed by tetrodotoxin (1 microM) but partially reduced by cyclo-(7-aminoheptanonyl-Phe-D-Trp-Lys-Thr[BZL]) (10 microM), a somatostatin antagonist. In conclusion, GABA enhances pancreatic Exocrine Secretion induced by secretagogues, which stimulate enzyme Secretion predominantly, via GABA(A) receptors in the rat pancreas. The enhancing effect of GABA is partially mediated by inhibition of islet somatostatin release. GABA does not modify the activity of intrapancreatic neurons.
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Roles of Gonadal Steroids on Exocrine Secretion of Isolated Perfused Rat Pancreas
The Korean Journal of Physiology and Pharmacology, 2020Co-Authors: H S Park, H J ParkAbstract:To clarify the roles of gonadal steroids on pancreatic Exocrine Secretion, effects of progesterone and estradiol-17β on spontaneous and secretagogue-induced Exocrine response of isolated perfused rat pancreas were investigated. Intra-arterial infusion of progesterone resulted in significant increase of the spontaneous pancreatic fluid and amylase Secretion dose-dependently. However, estradiol-17β did not exert any influence on spontaneous pancreatic Exocrine Secretion. Exogenous secretin, cholecystokinin (CCK), and acetylcholine markedly stimulated pancreatic fluid and amylase Secretion. Progesterone initially enhanced secretin-induced amylase Secretion, but this stimulatory response declined thereafter to basal value. Moreover, secretin-induced fluid Secretion was not affected by infusion of progesterone. Therefore, initial increase of Secretion-induced amylase Secretion by progesterone seems to be a non-specific action by washout effect of secretin. Estradiol-17β failed to change the secretin-induced fluid and amylase Secretion. Both progesterone and estradiol-17β did not exert any influence on CCK-induced fluid and amylase Secretion. Acetylcholine-induced Exocrine Secretion of isolated perfused pancreas also was not affected by intra-arterial infusion of progesterone or estradiol-17β. It is concluded from the above results that progesterone could enhance the spontaneous pancreatic fluid and amylase Secretion of isolated perfused rat pancreas through non-genomic short- term action, and that these effects could be masked by more potent stimulants such as secretin, CCK, and acetylcholine.
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γ-aminobutyric acid secreted from islet β-cells modulates Exocrine Secretion in rat pancreas
World Journal of Gastroenterology, 2006Co-Authors: Yong-deuk Park, H S Park, Guang Wu, H J ParkAbstract:AIM: To investigate the role of endogenous γ-amino-butyric acid (GABA) in pancreatic Exocrine Secretion. METHODS: The isolated, vascularly perfused rat pancreas was employed in this study to eliminate the possible influences of extrinsic nerves and hormones. Cholecystokinin (CCK; 10 pmol/L) was intra-arterially given to stimulate Exocrine Secretion of the pancreas. RESULTS: Glutamine, a major precursor of GABA, which was given intra-arterially at concentrations of 1, 4 and 10 mmol/L, dose-dependently elevated the CCK-stimulated Secretions of fluid and amylase in the normal pancreas. Bicuculline (10 μmol/L), a GABAA receptor antagonist, blocked the enhancing effect of glutamine (4 mmol/L) on the CCK-stimulated Exocrine Secretions. Glutamine, at concentrations of 1, 4 and 10 mmol/L, dose-dependently increased the GABA concentration in portal effluent of the normal pancreas. The effects of glutamine on the CCK-stimulated Exocrine Secretion as well as the GABA Secretion were markedly reduced in the streptozotocin-treated pancreas. CONCLUSION: GABA could be secreted from β-cells into the islet-acinar portal system after administration of glutainine, and could enhance the CCK-stimulated Exocrine Secretion through GABAA receptors. Thus, GABA in islet β-cells is a hormone modulating pancreatic Exocrine Secretion.
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Endogenous somatostatin inhibits interaction of insulin and cholecystokinin on Exocrine Secretion of isolated, perfused rat pancreas
Pancreas, 2002Co-Authors: H S Park, Yong-deuk Park, Hyo Seop Yoon, H J ParkAbstract:Introduction: Although somatostatin inhibits pancreatic Exocrine Secretion, the inhibitory mechanism of endogenous somatostatin is not clearly understood. Aim: To investigate the effect of endogenous somatostatin on the interaction between endogenous insulin and exogenous cholecystokinin (CCK) in Exocrine Secretion of the totally isolated, perfused rat pancreas. Methodology: Endogenous releases of somatostatin and insulin were induced by 18 mM glucose. Streptozotocin (75 mg/kg) or cysteamine (300 mg/kg) was injected into rats 24 hours before the experiment to deplete insulin or somatostatin in the pancreas. Results: Glucose (18 mM) enhanced CCK (10 pM)-stimulated Secretions of fluid and amylase in the normal pancreas, which was further elevated by a somatostatin antagonist. Exogenous insulin (100 nM) also enhanced CCK-stimulated Secretions in the streptozotocin-treated pancreas, which was also markedly increased by the somatostatin antagonist. The glucose (18 mM)-enhanced CCK-stimulated Secretions were much higher in the cysteamine-treated pancreas than in the normal pancreas, which was dose-dependently reduced by exogenous somatostatin (30, 100 pM). However, endogenous or exogenous somatostatin did not modify the pancreatic responses to CCK alone. Conclusion: Endogenous somatostatin inhibits the interaction of endogenous insulin and CCK on pancreatic Exocrine Secretion in the rat rather than reducing the action of CCK alone or endogenous release of insulin.
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Effects of γ-aminobutyric acid on secretagogue-induced Exocrine Secretion of isolated, perfused rat pancreas
American Journal of Physiology-gastrointestinal and Liver Physiology, 2000Co-Authors: H S Park, H J ParkAbstract:Because GABA and its related enzymes have been determined in β-cells of pancreas islets, effects of GABA on pancreatic Exocrine Secretion were investigated in the isolated, perfused rat pancreas. G...
William Y. Chey - One of the best experts on this subject based on the ideXlab platform.
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significant cholinergic role in secretin stimulated Exocrine Secretion in isolated rat pancreas
American Journal of Physiology-gastrointestinal and Liver Physiology, 1998Co-Authors: H S Park, William Y. Chey, Hyeok Yil Kwon, H J ParkAbstract:Effects of intrapancreatic cholinergic activation by electrical field stimulation (EFS) on secretin-stimulated pancreatic Exocrine Secretion were investigated in the totally isolated perfused rat pancreas. EFS at 15 V, 2 ms, and 8 Hz for 45 min markedly increased spontaneous pancreatic Secretion. This increase was completely inhibited by tetrodotoxin (1 μM) but not by hexamethonium (100 μM). Atropine (2 μM) significantly reduced the EFS-evoked volume flow and amylase output by 52% and 80%, respectively. EFS further increased the secretin (12 pM)-stimulated pancreatic Secretion of fluid and amylase. The increases of the two parameters were significantly suppressed by atropine by 28% and 72%, respectively. Interestingly, EFS significantly increased concentrations of somatostatin-like immunoreactivity in portal venous effluents. When pertussis toxin (200 ng/ml) or rabbit antisomatostatin serum (0.1 ml/10 ml; titer of 1:50,000) was intra-arterially administered, EFS further increased the secretin-stimulated pancreatic Secretion. In conclusion, the activation of intrapancreatic cholinergic neurons potentiated the secretin action on pancreatic Exocrine Secretion in the rat. This potentiating effect was significantly reduced by local somatostatin released during EFS that activated intrapancreatic cholinergic tone.
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Effect of intraduodenai infusion of tocamphyl on pancreatic Exocrine Secretion and gastrointestinal hormone release in rats
International Journal of Pancreatology, 1994Co-Authors: Mikio Imamura, Hidemi Yamauchi, William Y. CheyAbstract:Tocamphyl is a synthetic choleretic that is derived from a root extract ofCurcuma longa, L. We investigated the effect of tocamphyl on pancreatic Exocrine Secretion and bile flow, and on the release of some gastrointestinal hormones, by administering it intraduodenally using anesthetized rats. Tocamphyl stimulated pancreatic Exocrine Secretion in terms of volume and amylase output in a dose-related manner. Neither a CCK-receptor antagonist, CR1505 (loxiglumide), nor atropine sulfate infused intravenously suppressed the stimulatory effects of tocamphyl on pancreatic Exocrine Secretion and bile flow. The stimulatory effect on bile flow was stronger than that on pancreatic Exocrine Secretion. Plasma secretin levels were augmented with the increasing doses of tocamphyl, but CCK levels were not. These results indicate that intraduodenally administered tocamphyl stimulates pancreatic Exocrine Secretion and bile flow, and suggest that the stimulatory action is, at least in part, mediated by secretin, but not by either CCK or the cholinergic pathway.
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Effect of digested protein on pancreatic Exocrine Secretion and gut hormone release in the dog.
Pancreas, 1994Co-Authors: Masaya Moriyasu, T.m. Chang, William Y. CheyAbstract:The hormonal mechanisms mediating protein-stimulated pancreatic Exocrine Secretion were investigated in four conscious dogs with gastric cannulas and Thomas duodenal cannulas. Pancreatic juice was collected by direct cannulation of the main pancreatic duct in response to intraduodenal infusates prepared with cooked beef liver. When the homogenized liver was administered intraduodenally, cholecystokinin (CCK) in plasma significantly increased. This increase was accompanied by a significant increase in pancreatic Exocrine Secretion, including volume, bicarbonate, and protein output. The liver homogenate incubated with pancreatic enzymes further increased both plasma CCK and Exocrine pancreatic Secretion. However, plasma secretin was not affected by the protein digests. Intravenous administration of loxiglumide at the rate of 5.0 and 10.0 mg/kg/h resulted in a significant decrease in the stimulated pancreatic Secretion of fluid, bicarbonate, and protein. The study indicates that endogenous CCK released by protein digests exerts not only enzyme Secretion but also bicarbonate Secretion in dogs.
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Regulation of pancreatic Exocrine Secretion
International Journal of Pancreatology, 1991Co-Authors: William Y. CheyAbstract:The Exocrine pancreas secretes throughout 24 hours. In both interdigestive and postprandial states, pancreatic Secretion is regulated by neural and hormonal actions, and neurohormonal interactions. At the turn of this century, the prevailing theory of Pavlov (1) that pancreatic Exocrine Secretion was exclusively regulated by secretory fibers in both vagi and splanchnic nerves was refuted by Bayliss and Starling in 1902, who put forward their hypothesis that pancreatic Secretion was stimulated by a circulating hormone, “secretin,” which was released by hydrochloric acid from the duodenal mucosa (2). Soon, Pavlov conceded to the hypothesis of Bayliss and Starling. Pavlov adopted the theory of a dual mechanism—nervous and hormonal—of the regulation of pancreatic Secretion. In recent decades, explosions of new information about old and newly discovered gut hormones or peptides and neuropeptides have resulted in a better understanding of the regulatory mechanism of the Exocrine pancreas, and also opened new, exciting frontiers in the investigations of the physiology and patho-physiology of pancreatic Secretion.
Kyoko Miyasaka - One of the best experts on this subject based on the ideXlab platform.
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central administration of ghrelin stimulates pancreatic Exocrine Secretion via the vagus in conscious rats
Japanese Journal of Physiology, 2003Co-Authors: Norikazu Sato, Akihiro Funakoshi, Setsuko Kanai, Mieko Kurosawa, Saeko Takano, Kyoko MiyasakaAbstract:Ghrelin, a novel growth-hormone releasing peptide, was originally isolated from rat and human stomach. Immunohistochemical analyses revealed that ghrelin-immunoreactive neurons were localized in the hypothalamic arcuate nucleus. The function of the digestive organs is controlled from the central nervous system, and the vagus nerve plays an important role. Intracerebroventricular and intravenous administration of ghrelin significantly increased gastric acid Secretion, and its effect was abolished by vagotomy. In the present study, the effect of centrally injected ghrelin on pancreatic Exocrine Secretion was examined in conscious rats. Moreover, an electrophysiologic study was conducted in anesthetized rats to examine whether the excitation of vagal efferent nerve could be induced by ghrelin. To determine the pancreatic Exocrine Secretion, rats were prepared with cannulae draining bile and pancreatic juice separately. The experiments were conducted in conscious rats on day 4 or 5 after the operation. To exclude the involvement of gastric acid, a proton pump inhibitor omeprazole (5 μmol/kg) was administered into the duodenum 1 h before ghrelin injection. An intracerebroventricular administration of ghrelin (12, 60, and 300 pmol/10 μl) significantly increased pancreatic fluid and protein output in a dose-dependent manner. Pretreatment with the ganglion blocker hexamethonium and with atropine completely abolished the stimulatory effect of central ghrelin. In contrast, an intravenous injection of ghrelin (300 pmol/10 μl) had no effect. Centrally administered ghrelin stimulated the vagal efferent nerve in anesthetized rats. In conclusion, centrally administered ghrelin stimulates pancreatic Exocrine Secretion through the vagal efferent nerve, and the stimulatory action is independent of gastric acid Secretion.
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central orexin a stimulates pancreatic Exocrine Secretion via the vagus
Pancreas, 2002Co-Authors: Kyoko Miyasaka, Masao Masuda, Setsuko Kanai, Norikazu Sato, Mieko Kurosawa, Akihiro FunakoshiAbstract:Introduction: Digestive organs are controlled from the central nervous system, and the vagus nerve plays an important role. Orexins are recently purified neuropeptides localized in neurons within the lateral hypothalamus. Aim: To examine the effects of centrally injected Orexin-A and B on pancreatic Exocrine Secretion in conscious rats. Methodology: Rats were prepared with cannulae draining bile and pancreatic juice separately. The experiments were conducted without anesthesia on day 4 or 5 after the operation. Results: Intracerebroventricular administration of Orexin-A (0.25, 0.5, and 1.0 nmol) significantly increased pancreatic fluid and protein output in a dose-dependent manner. A significant stimulatory effect of Orexin-B was not observed. Pretreatment with the ganglion blocker hexamethonium and with atropine completely abolished the stimulatory effect of central Orexin-A. Central Orexin-A significantly increased pancreatic Secretion after pretreatment with omeprazole. Intravenous injection of Orexin-A had no effect. Centrally administered Orexin-A stimulated the vagal efferent nerve in anesthetized rats. Conclusions: Centrally administered Orexin-A stimulates pancreatic Exocrine Secretion through the vagal efferent nerve, and the stimulatory action is independent of gastric acid Secretion.
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Somatostatin inhibits pancreatic Exocrine Secretion centrally via sympathetic nerves in conscious rats
Journal of The Autonomic Nervous System, 1995Co-Authors: Masao Masuda, Kyoko Miyasaka, Setsuko Kanai, Akihiro FunakoshiAbstract:Somatostatin is known to be a potent inhibitor of pancreatic Exocrine Secretion, but the mechanism of its effect is not fully understood. The mechanism of the inhibition by centrally administered somatostatin was examined in conscious rats. Rats were prepared with cannulae draining bile and pancreatic juice separately, and with a duodenal cannula, an extrajugular vein cannula and a cerebroventricular cannula. Somatostatin was injected into the left lateral ventricle, and the inhibitory mechanism was examined using vagotomized rats and various drugs that affect sympathetic neurons. Intracerebroventricular administration of somatostatin significantly inhibited pancreatic Exocrine Secretion stimulated by bile-pancreatic juice diversion. The inhibitory effect was not abolished by vagotomy, pretreatment with propranolol, but was abolished by pretreatment with hexamethonium or phentolamine. The plasma level of somatostatin after its intracerebroventricular administration increased 3-fold, but its intravenous infusion at a rate giving a similar plasma somatostatin level to that produced by its intracerebroventricular injection, had no significant effect on pancreatic Secretion. These results suggest that somatostatin inhibits pancreatic Exocrine Secretion centrally via sympathetic efferent nerves and that α-adrenergic receptors have an important role in its inhibitory action.
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Cholinergic Stimulatory Effect of Intragastric Administration of a Prostaglandin E2 Analogue on Pancreatic Exocrine Secretion in Conscious Rats
Pancreas, 1995Co-Authors: Masao Masuda, Kyoko Miyasaka, Akihiro FunakoshiAbstract:The effect of a long-acting, potent synthetic analogue of prostaglandin E 2 , enprostil, on pancreatic Exocrine Secretion was examined in conscious rats. Rats were prepared with cannulae draining bile and pancreatic juice separately. Pancreatic Exocrine Secretion was increased by intragastric administration of enprostil but inhibited by its intravenous administration. The pancreatic response to intragastric administration of enprostil was not inhibited by the administration of cholecystokinin antagonist or secretin antibody, or by bilateral vagotomy, but was completely abolished by atropine. Therefore, intragastric administration of enprostil seemed to stimulate pancreatic Exocrine Secretion via a peripheral gastro-(entero)-pancreatic reflex
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Effect of ursodeoxycholate on pancreatic Exocrine Secretion in vitro and in vivo study
The Japanese journal of gastro-enterology, 1992Co-Authors: Hirotsugu Shinozaki, Akihiro Funakoshi, Kyoko Miyasaka, Kenichi KitaniAbstract:In the present study, we examined the effect of ursodeoxycholate (UDCA) and it's taurine conjugate (TUDC) on rat pancreatic Exocrine Secretion using dispersed pancreatic acini (in vitro) and conscious rats (in vivo). In in vitro study 300 microM UDCA significantly increased 10(-12)-10(-9) M CCK-8 stimulated amylase release and change of intracellular Ca2+ concentration, but TUDC did not have these effects. In in vivo study intraduodenal infusion of UDCA but not TUDC stimulated pancreatic Exocrine Secretion. Intravenous infusion of secretin antibody decreased bicarbonate output, however, this increase was not prevented by CCK antagonist. Thus, it was suggested that UDCA has direct action on pancreatic acini and UDCA infused intraduodenally stimulates pancreatic Secretion, possibly via the release of a secretin-like substance. The taurine conjugate has weak bioactivity on pancreatic Exocrine Secretion in both in vitro and in vivo.
Akihiro Funakoshi - One of the best experts on this subject based on the ideXlab platform.
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central administration of ghrelin stimulates pancreatic Exocrine Secretion via the vagus in conscious rats
Japanese Journal of Physiology, 2003Co-Authors: Norikazu Sato, Akihiro Funakoshi, Setsuko Kanai, Mieko Kurosawa, Saeko Takano, Kyoko MiyasakaAbstract:Ghrelin, a novel growth-hormone releasing peptide, was originally isolated from rat and human stomach. Immunohistochemical analyses revealed that ghrelin-immunoreactive neurons were localized in the hypothalamic arcuate nucleus. The function of the digestive organs is controlled from the central nervous system, and the vagus nerve plays an important role. Intracerebroventricular and intravenous administration of ghrelin significantly increased gastric acid Secretion, and its effect was abolished by vagotomy. In the present study, the effect of centrally injected ghrelin on pancreatic Exocrine Secretion was examined in conscious rats. Moreover, an electrophysiologic study was conducted in anesthetized rats to examine whether the excitation of vagal efferent nerve could be induced by ghrelin. To determine the pancreatic Exocrine Secretion, rats were prepared with cannulae draining bile and pancreatic juice separately. The experiments were conducted in conscious rats on day 4 or 5 after the operation. To exclude the involvement of gastric acid, a proton pump inhibitor omeprazole (5 μmol/kg) was administered into the duodenum 1 h before ghrelin injection. An intracerebroventricular administration of ghrelin (12, 60, and 300 pmol/10 μl) significantly increased pancreatic fluid and protein output in a dose-dependent manner. Pretreatment with the ganglion blocker hexamethonium and with atropine completely abolished the stimulatory effect of central ghrelin. In contrast, an intravenous injection of ghrelin (300 pmol/10 μl) had no effect. Centrally administered ghrelin stimulated the vagal efferent nerve in anesthetized rats. In conclusion, centrally administered ghrelin stimulates pancreatic Exocrine Secretion through the vagal efferent nerve, and the stimulatory action is independent of gastric acid Secretion.
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central orexin a stimulates pancreatic Exocrine Secretion via the vagus
Pancreas, 2002Co-Authors: Kyoko Miyasaka, Masao Masuda, Setsuko Kanai, Norikazu Sato, Mieko Kurosawa, Akihiro FunakoshiAbstract:Introduction: Digestive organs are controlled from the central nervous system, and the vagus nerve plays an important role. Orexins are recently purified neuropeptides localized in neurons within the lateral hypothalamus. Aim: To examine the effects of centrally injected Orexin-A and B on pancreatic Exocrine Secretion in conscious rats. Methodology: Rats were prepared with cannulae draining bile and pancreatic juice separately. The experiments were conducted without anesthesia on day 4 or 5 after the operation. Results: Intracerebroventricular administration of Orexin-A (0.25, 0.5, and 1.0 nmol) significantly increased pancreatic fluid and protein output in a dose-dependent manner. A significant stimulatory effect of Orexin-B was not observed. Pretreatment with the ganglion blocker hexamethonium and with atropine completely abolished the stimulatory effect of central Orexin-A. Central Orexin-A significantly increased pancreatic Secretion after pretreatment with omeprazole. Intravenous injection of Orexin-A had no effect. Centrally administered Orexin-A stimulated the vagal efferent nerve in anesthetized rats. Conclusions: Centrally administered Orexin-A stimulates pancreatic Exocrine Secretion through the vagal efferent nerve, and the stimulatory action is independent of gastric acid Secretion.
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Somatostatin inhibits pancreatic Exocrine Secretion centrally via sympathetic nerves in conscious rats
Journal of The Autonomic Nervous System, 1995Co-Authors: Masao Masuda, Kyoko Miyasaka, Setsuko Kanai, Akihiro FunakoshiAbstract:Somatostatin is known to be a potent inhibitor of pancreatic Exocrine Secretion, but the mechanism of its effect is not fully understood. The mechanism of the inhibition by centrally administered somatostatin was examined in conscious rats. Rats were prepared with cannulae draining bile and pancreatic juice separately, and with a duodenal cannula, an extrajugular vein cannula and a cerebroventricular cannula. Somatostatin was injected into the left lateral ventricle, and the inhibitory mechanism was examined using vagotomized rats and various drugs that affect sympathetic neurons. Intracerebroventricular administration of somatostatin significantly inhibited pancreatic Exocrine Secretion stimulated by bile-pancreatic juice diversion. The inhibitory effect was not abolished by vagotomy, pretreatment with propranolol, but was abolished by pretreatment with hexamethonium or phentolamine. The plasma level of somatostatin after its intracerebroventricular administration increased 3-fold, but its intravenous infusion at a rate giving a similar plasma somatostatin level to that produced by its intracerebroventricular injection, had no significant effect on pancreatic Secretion. These results suggest that somatostatin inhibits pancreatic Exocrine Secretion centrally via sympathetic efferent nerves and that α-adrenergic receptors have an important role in its inhibitory action.
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Cholinergic Stimulatory Effect of Intragastric Administration of a Prostaglandin E2 Analogue on Pancreatic Exocrine Secretion in Conscious Rats
Pancreas, 1995Co-Authors: Masao Masuda, Kyoko Miyasaka, Akihiro FunakoshiAbstract:The effect of a long-acting, potent synthetic analogue of prostaglandin E 2 , enprostil, on pancreatic Exocrine Secretion was examined in conscious rats. Rats were prepared with cannulae draining bile and pancreatic juice separately. Pancreatic Exocrine Secretion was increased by intragastric administration of enprostil but inhibited by its intravenous administration. The pancreatic response to intragastric administration of enprostil was not inhibited by the administration of cholecystokinin antagonist or secretin antibody, or by bilateral vagotomy, but was completely abolished by atropine. Therefore, intragastric administration of enprostil seemed to stimulate pancreatic Exocrine Secretion via a peripheral gastro-(entero)-pancreatic reflex
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Effect of ursodeoxycholate on pancreatic Exocrine Secretion in vitro and in vivo study
The Japanese journal of gastro-enterology, 1992Co-Authors: Hirotsugu Shinozaki, Akihiro Funakoshi, Kyoko Miyasaka, Kenichi KitaniAbstract:In the present study, we examined the effect of ursodeoxycholate (UDCA) and it's taurine conjugate (TUDC) on rat pancreatic Exocrine Secretion using dispersed pancreatic acini (in vitro) and conscious rats (in vivo). In in vitro study 300 microM UDCA significantly increased 10(-12)-10(-9) M CCK-8 stimulated amylase release and change of intracellular Ca2+ concentration, but TUDC did not have these effects. In in vivo study intraduodenal infusion of UDCA but not TUDC stimulated pancreatic Exocrine Secretion. Intravenous infusion of secretin antibody decreased bicarbonate output, however, this increase was not prevented by CCK antagonist. Thus, it was suggested that UDCA has direct action on pancreatic acini and UDCA infused intraduodenally stimulates pancreatic Secretion, possibly via the release of a secretin-like substance. The taurine conjugate has weak bioactivity on pancreatic Exocrine Secretion in both in vitro and in vivo.